Editorial Focus Mesolimbic dopamine in obesity and diabetes

MONOAMINERGIC NEUROTRANSMITTER dopamine plays a critical role in various vital functions, including hormonal regulation, reward, emotions, and food intake. Multiple aspects of food intake that include food selection, satiety, and energy expen-diture could be modulated by changes in central dopaminergic transmission (3, 11). Several lines of research indicate that abnormal dopaminergic neurotransmission could be involved in pathophysiological processes leading to obesity. Most of these studies are focused on the hypothalamic dopamine trans-mission that is believed to play a pivotal role in the guidance of fuel flux and energy homeostasis (13). Generally, these investigations have indicated a decreased dopaminergic signal-ing in obese subjects (13). For example, dopamine D2 recep-tors were found to be lower in several brain regions in both obese experimental animals and humans, and it has been observed that dopamine D2 agonist bromocriptine can exert favorable metabolic changes in seasonal obesity (13). In line with this contention, obesity is one of the best known side-effect of antipsychotic drugs that exert their actions mostly via antagonism of D2 dopamine receptors (2). It should be noted, however, that there is also evidence, indicating that in brain mesolimbic structures responsible for motivation, reward, and emotions, particularly in the nucleus accumbens, a situation may be completely different and obesity can be accompanied with an increased dopamine signaling that could determine an increased motivation for food consumption (9). It has become increasingly clear that food shares the ability of many drugs of abuse to activate common reward circuits such as mesolimbic dopamine system. Furthermore, obesity, like drug addiction, might be considered as a special case of the consequences of ingestive behavior gone awry (11, 15)